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目的探讨氯化钆(Gadolinium chloride,Gd Cl3)在细菌脂多糖(Lipopolysaccharide,LPS)引起肝脏损伤的影响及其机制。方法将MT基因敲除小鼠(MT-/-)及与之对应的野生型小鼠(MT+/+)各分为4组:生理盐水对照组、LPS染毒组、Gd Cl3组和Gd Cl3预处理+LPS染毒组。动物腹腔注射LPS(10 mg/kg,腹腔注射)或生理盐水(NS,腹腔注射),此前24 h给予Gd Cl3(10 mg/kg,尾静肪注射)或NS预处理。注射LPS后24 h测定血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)活力以及一氧化氮(NO)含量,镉饱和法测定肝脏金属硫蛋白(MT)含量,进行肝组织病理学检查,判定不同处理对MT-/-小鼠及MT+/+小鼠肝脏影响的差异。结果注射LPS后,MT-/-小鼠及MT+/+小鼠血ALT、AST活力,血NO含量均较对照组升高,两种小鼠肝组织均出现大量炎性细胞浸润、肝细胞浊肿、空泡变性、灶性液化坏死、星状细胞增生。组织病理学检查结果显示MT-/-小鼠肝组织损伤程度较MT+/+小鼠更为严重。氯化钆、LPS均可以诱导MT+/+小鼠肝脏MT生成。Gd Cl3预处理可以同时降低LPS对MT-/-小鼠及MT+/+小鼠血ALT,AST活力,血NO含量的影响,可以减轻LPS对两种小鼠肝组织病理学损伤。结论 Gd Cl3预处理可以有效减轻由LPS引起的肝脏损伤,MT通过其对Kuffer细胞的抑制作用保护LPS引起的肝脏损伤。
Objective To investigate the effect and mechanism of Gadolinium chloride (Gd Cl3) on hepatic injury induced by bacterial lipopolysaccharide (LPS). Methods MT gene knockout mice (MT - / -) and corresponding wild type mice (MT + / +) were divided into four groups: saline control group, LPS group, Gd Cl3 group and Gd Cl3 Pretreatment + LPS exposure group. The animals were intraperitoneally injected with LPS (10 mg / kg ip) or saline (NS injected intraperitoneally) given Gd Cl3 (10 mg / kg, tail fat injection) or NS pretreatment 24 h before. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and nitric oxide (NO) were measured at 24 h after LPS injection. Liver metallothionein (MT) Neutrophil test, to determine the different treatment of MT - / - mice and MT + / + mice liver differences. Results After LPS injection, ALT, AST activity and blood NO levels were increased in both MT - / - and MT + / + mice compared with the control group. There were a large number of inflammatory cell infiltration and hepatocyte turbidity in both liver tissues Swollen, vacuolar degeneration, focal liquefaction necrosis, stellate cell proliferation. Histopathological examination showed that liver damage in MT - / - mice was more severe than that in MT + / + mice. Both gadolinium chloride and LPS can induce liver MT production in MT + / + mice. GdCl3 preconditioning could reduce the effect of LPS on ALT, AST activity and blood NO content in MT - / - mice and MT + / + mice, and alleviate the pathological damage induced by LPS in both groups. Conclusion Gd Cl3 pretreatment can effectively reduce the liver injury caused by LPS. MT protects liver injury induced by LPS through its inhibitory effect on Kuffer cells.